CLINICAL OBSTETRICS AND GYNECOLOGY

Volume 55, Number 4, 893903

r 2012, Lippincott Williams & Wilkins

Pathogenesis,
Diagnosis, and
Management
of Severe Pelvic
Inflammatory Disease
and Tuboovarian
Abscess
CATHERINE A. CHAPPELL, MD and
HAROLD C. WIESENFELD, MD, CM
Magee-Womens Hospital of UPMC, University of Pittsburgh,
Pittsburgh, Pennsylvania

Abstract: Severe pelvic inflammatory disease and

tuboovarian abscesses (TOAs) are common pelvic
infections requiring inpatient admission. There are
few large randomized trials guiding appropriate clin-
ical management of TOA, including antibiotic selec-
tion and timing of surgical management and drainage.
The pathogenesis, diagnosis, and management of se-
vere pelvic inflammatory disease and TOA are sum-
marized and reviewed from the most current literature.
Key words: pelvic inflammatory disease, PID,
tuboovarian abscess, TOA, management
Correspondence: Harold C. Wiesenfeld, MD, CM,
Magee-Womens Hospital of UPMC, University of
Pittsburgh, Pittsburgh, PA. E-mail: hwiesenfeld@
mail.magee.edu
H.C.W. is currently receiving research funding from
MethylGene Inc.; C.A.C. declares nothing to disclose.
Introduction
Pelvic inflammatory disease (PID) is a
polymicrobial ascending infection that
causes inflammation of the upper genital
tract, including endometritis, salpingitis,
pelvic peritonitis, and occasionally lead-
ing to tuboovarian abscess (TOA) forma-
tion.1 PID can be classified as acute,
subacute, or subclinical. The healthcare
burden of PID is generally underesti-
mated because of cases of undiagnosed
subclinical PID. Even so, PID accounts
for 2.5 million outpatient visits, 200,000
hospitalizations, and 100,000 surgical
procedures.2 Annually over 1 billion dol-
lars was spent on the treatment of PID.
Another 1 billion dollars was spent on
care for the sequelae of PID such as

CLINICAL OBSTETRICS AND GYNECOLOGY / VOLUME 55 / NUMBER 4 / DECEMBER 2012

www.clinicalobgyn.com | 893
894 Chappell and Wiesenfeld
chronic pelvic pain, infertility, and ectopic
pregnancy. This review will focus on acute
and severe cases of PID, including those
complicated by TOA.
Epidemiology and Risk Factors
The incidence of PID correlates with the
incidence of sexually transmitted diseases,
which increased in the 1970s and peaked
in 1982 with an estimated 1 million cases
and 14.2% prevalence of PID treatment
among reproductive-aged women in the
United States.3,4 However, generally the
incidence and prevalence of PID is diffi-
cult to assess because of the lack of report-
ing requirement for PID, high rates of
subclinical PID, increasing rates of out-
patient management, and inaccuracies in
diagnosis.
Several risk factors for the develop-
ment of PID have been identified, while
others remain controversial. PID is highly
associated with younger age of coitarche,
multiple sexual partners, nonuse of bar-
rier contraception, and infection with
chlamydia or gonorrhea.5 The Dalkon
Shield, an intrauterine device (IUD) that
is no longer available, increased users risk
of PID by a wicking effect of its multifila-
ment string that allowed microbes to as-
cend into the upper genital tract from the
vagina.6 Modern IUDs do not seem to
increase the risk of development of PID
beyond the risk associated with insertion
of the device.7,8 Case-controlled studies
have shown an association between vagi-
nal douching and PID.911 Hypothesized
mechanisms for this association have in-
cluded the introduction of vaginal mi-
crobes into the upper genital tract by the
force of the douche fluid or the shift of
protective microbiological flora.
It is unclear why some women with PID
develop TOA, whereas the majority of
women do not. Formation of TOA may
be related to prior PID infection, delay in
treatment, or virulence factors of the
pathogens.12 Among hospitalized patients
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with PID approximately one third have
TOA.12 An increase in the prevalence of
TOAs among women hospitalized for PID
might be related to increasing frequency
and acceptability of outpatient treatment
of PID, thus leading to hospitalization in
only severe cases of PID and those with
TOAs.13 The risk factors for TOA are
similar to those of PID, including multiple
sex partners, age between 15 and 25 years,
and a prior history of PID. Women with
human immunodeficiency virus infection
may be more likely to develop TOA com-
pared with women negative for human
immunodeficiency virus.14,15
Pathogenesis
PID is caused by an ascending infection of
lower genital tract organisms from the
vagina or cervix into the upper tract,
including the uterus, fallopian tubes, and
peritoneal cavity. Up to 75% of cases
occur during the follicular phase of the
menstrual cycle.16 Similarly, a high estro-
gen environment along with the presence
of cervical ectopy found in adolescence
facilitates the attachment of Chlamydia
trachomatis and Neisseria gonorrhoeae,
which may contribute to the higher rates
of PID among young women.17
TOAs are also caused by an ascending
infection to the fallopian tube causing
endothelial damage and edema of the
infundibulum resulting in tubal blockage.
The ovary may become involved presum-
ably by invasion of organisms through the
ovulation site. Eventually the separation
between the ovary and fallopian tube is
lost. Necrosis inside this complex mass
may result in 1 or more abscess cavities
and an anaerobic growth environment.12
A TOA may also form from local spread
of infection associated with uncontrolled
inflammatory disease of the bowel, ap-
pendicitis, or adnexal surgery. It is impor-
tant to note that TOAs, unlike other
types of abscesses, occur between organs
rather than confined inside an organ. The

adherence of adjacent pelvic structures,
such as the omentum and bowel, might
serve a host defense mechanism to contain
the inflammatory process within the pel-
vis. This could be a reason that some
women with TOA are not overtly sick
with an elevated white cell count or fever.
Microbiological Etiology
The organisms associated with upper gen-
ital tract infection have been identified
using endometrial biopsy, culdocentesis,
and laparoscopy. PID has been deter-
mined to be polymicrobial in nature, be-
cause multiple different bacteria have
been isolated from the upper genital tract
in women with PID.18 These bacteria can
be artificially divided into 2 categories:
sexually transmitted pathogens and lower
genital tract flora. Sexually transmitted
infections, such as N. gonorrhoeae, Chla-
mydia trichomatis, and Mycoplasma gen-
italium, have all been identified from the
cervix, endometrium, and fallopian tubes
from women with acute sapingitis diag-
nosed by laporoscopy.1921 However, en-
dogenous, bacterial vaginosis-associated
lower genital tract organisms, such as
Prevotella species, Peptostreptococci sp.,
Gardnerella vaginalis, Escherichia coli,
Haemophilus influenza, and aerobic strep-
tococci are found in a high percentage of
PID cases.22,23
Like PID, TOAs are also polymicrobial
infections with a mixture of anaerobic,
aerobic, and facultative organisms. Sexu-
ally transmitted pathogens are infre-
quently isolated from TOAs. Gonorrhea
was isolated from only 3.8% of 53 TOA
aspirates, despite an overall recovery rate
of 31% from the cervix. There are no
published reports isolating C. trichomatis
from an abscess cavity. The role of gonor-
rhea and chlamydia may be limited to
antecedent infections such as cervicitis
or PID; and gonorrhea may facilitate
invasion of the upper genital tract by
lower genital tract flora.12 Alternatively,
Severe Pelvic Inflammatory Disease 895
the inflammatory environment of the ab-
scess cavity may make it difficult to isolate
these organisms by culture if they are
present. The most common organisms
isolated for TOAs are E. coli, Bacteriodes
fragilis, Bacteriodes species, Peptostrepto-
coccus, Peptococcus, and aerobic strepto-
coccus.12,24 Importantly, E. coli is a
common isolate in women with ruptured
TOAs and a frequent cause of Gram-
negative sepsis.25 TOAs that occur in
women with long-term use of an IUD
are often associated with Actinomyces
israelii.26,27
Diagnosis of PID and TOA
Acute PID is difficult to diagnose because
of the wide variation of signs and symp-
toms. There is no single subjective com-
plaint, physical examination finding, or
laboratory finding that is highly sensitive
or specific for the diagnosis of PID. The
diagnosis of PID is imprecise because
clinicians must consider a combination
of factors to make the diagnosis. The
clinical diagnosis of PID has a positive
predictive value of only 65% to 90% even
in the most experienced hands.28,29 How-
ever, delay in diagnosis and treatment can
lead to the postinflammatory sequelae of
the upper genital tract, such as infertility,
ectopic pregnancy, and chronic pelvic
pain. Therefore, empiric treatment should
be initiated in women at risk for sexually
transmitted diseases if they are experienc-
ing pelvic or lower abdominal pain, if
other illnesses have been ruled out and if
they have cervical motion tenderness, ute-
rine tenderness, or adnexal tenderness. In
addition, 1 or more of the following cri-
teria enhances the specificity of the diag-
nosis: fever, abnormal cervical or vaginal
mucopurulent discharge, presence of
abundant white blood cells on saline mi-
croscopy, elevated erythrocyte sedimen-
tation rate, elevated C-reactive protein,
and cervical infection with N. gonorrhoeae
or C. trichomatis.1
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896 Chappell and Wiesenfeld
The most common clinical manifesta-
tions of surgically confirmed TOA are
abdominal or pelvic pain (>90%), fever
(50%), vaginal discharge (28%), nausea
(26%), and abnormal vaginal bleeding
(21%). Of these cases, 23% of patients
had normal white blood cell counts.24 It is
very important to realize that the absence
of fever and an elevated white count does
not preclude the diagnosis of TOA. The
diagnosis of TOA requires the recognition
of an inflammatory mass. However, these
masses can be missed on physical exami-
nation because pain precludes an ad-
equate examination. Therefore, clinicians
should have a low threshold for obtaining
imaging in a woman with PID, especially
when the woman is acutely ill, when there
is exquisite tenderness on examination,
when palpation of the adnexa bimanual
examination is suboptimal, or when the
patient lacks clinical response to antibiotic
therapy.
Imaging of TOA
Transvaginal ultrasound and pelvic com-
puted tomography (CT) are the most
common imaging modalities used to de-
tect TOA. Transvaginal ultrasound is
considered the first-line imaging modality
because it provides excellent imaging of
the upper genital tract, is relatively inex-
pensive, and does not expose the patient
to radiation. Ultrasound finding sugges-
tive of PID includes enlarged ovarian
volumes or polycystic ovaries, thickened
fluid-filled ovaries with incomplete sep-
tum or the cog wheel sign, and complex
free fluid in the cul-de-sac.30 With more
severe or progressive PID, the anatomic
distinction between the ovary and the
fallopian tube can no longer be identified,
forming a TOA.31 TOAs are character-
ized by a complex multilocular cystic mass
with thick irregular walls, partitions, and
internal echoes.12,24,32 Figure 1 shows an
ultrasound image of a pyosalpinx where
complex fluid inside the fallopian tube
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FIGURE 1. Ultrasound image of pyosalpinx.
and significant tubal wall thickening can
be noted. Pelvic CT is preferred for wom-
en where the diagnosis is uncertain and
there is concern for a coexisting malig-
nancy or gastrointestinal pathology, such
as appendicitis or diverticulitis. CT might
have slight diagnostic advantages to ul-
trasound. Specifically it may have in-
creased sensitivity to detect a TOA (78%
to 100% vs. 75% to 82%, respectively)
and improved specificity (100% to 91%)
compared with an ultrasound.3335 In
a case series of 22 patients with TOA
reported by Hiller and colleagues, the
most common CT findings were unilateral
location (73%), multilocularity (89%), and
thick, uniform, enhancing walls. Less com-
mon findings included bowel thickening
(59%), uteral sacral ligament thickening
(64%), and pylosalpinx (50%).36 Figure 2
shows a CT image of left pyosalpinx
and a right TOA. Magnetic resonance
imaging has not been studied greatly in
the diagnosis of TOA. It remains unclear
if the great cost associated with this imag-
ing modality is worth any additional diag-
nostic or clinical information provided
by it.
Treatment
Treatment of PID begins with rapid
initiation of broad-spectrum antibiotics

FIGURE 2. Computed tomographic image of
pyosalpinx and tuboovarian abscess.
targeted against the most common patho-
gens, as described in the preceding para-
graphs. The efficacies of these regimens
have been determined by clinical or mi-
crobiological cure in short-term studies,
not by prevention of long-term complica-
tions. Women with mild or moderate PID
achieved clinical outcomes with outpa-
tient oral antibiotics similar to those with
inpatient IV antibiotics.37
The decision for hospitalization should
be based on provider judgment or any of
the following criteria as recommended by
the Centers for Disease Control and
Prevention:
 Surgical emergencies cannot be
excluded;
 Pregnancy;
 Lack of response to oral antibiotics;
 Inability to follow or tolerate an out-
patient oral regimen;
 Severe illness, nausea and vomiting, or
high fever;
 Presence of TOA.1
Women with TOA should have direct
inpatient observation for 24 hours be-
cause of risk of abscess rupture and sepsis.
Patients with clinically severe PID or
who meet the above criteria should be
admitted to the hospital and receive
parenteral antibiotics. In addition, medi-
cations for symptom relief of pain, nausea
or vomiting, and fever should also be
Severe Pelvic Inflammatory Disease 897
initiated upon admission. Fluid resuscita-
tion should also be considered in patients
that are unable to tolerate oral intake.
The Centers for Disease Control and Pre-
vention recommends the following intra-
venous (IV) antibiotics, which have been
shown to achieve clinical cure in>90% of
patients with acute PID:
 IV cefotetan or IV cefoxitin plus oral or
IV doxycycline
 IV clindamycin plus IV gentamicin
 Alternative: ampicillin/sulbactam plus
doxycyline.1
These regimens provide broad coverage
for not only N. gonorrhoeae, C. trichoma-
tis, and M. genitalium, but also for strep-
tococcus, Gram-negative enteric bacteria
(E. coli, Klebsiella spp., and Proteus spp.),
and bacteria vaginosis-associated anaero-
bic organisms.3842 The cephalosporin-
based regimen is preferred because of
improved tolerability. In the case of a
severe penicillin allergy, clindamycin plus
gentamicin is recommended.
For the treatment of TOA, when com-
paring the first-line parenteral antibiotic
regimens, none of the regimens have been
shown to be superior.12,24,43 We recom-
mend that antibiotic should be based on
the ability of the antibiotic to penetrate
the abscess cavity, the stability of the
agent in an acidic and hypoxic environ-
ment, and local susceptibility of Gram-
negative aerobic and anaerobic bacteria,
specifically E. coli, to the agent. Regimens
including clindamycin, metronidazole,
and cefoxitin should be considered in the
presence of TOA because they have been
shown to have superior abscess wall pen-
etration and activity within the cavity in
animal models.44 Reed et al45 showed in
a series of 232 patients with TOA that
clindamycin plus gentamicin (68%) was
more effective than penicillin and genta-
micin (49%) for reduction of TOA size,
highlighting the importance of anaerobic
coverage with clindamycin. However,
amnioglycosides have reduced activity
in acidic, anaerobic environments with
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898 Chappell and Wiesenfeld
purulent debris.46 McNeeley et al47 showed
that the combination of ampicillin, genta-
micin, and clindamycin (87.5%) has an
improved cure rate as compared with clin-
damycin and gentamicin alone (47%).
Therefore, for the treatment of TOA,
an extended-spectrum cephalosporin for
the coverage of Gram-negative organisms
(rather than an aminoglycoside) combined
with clindamycin or metronidazole is a
good option.
Guidelines for the treatment of intra-
abdominal infections have recommended
that when resistance for a specific anti-
biotic exceeds >10% to 20% of all iso-
lates, then a change in the recommended
antibiotic should occur. For this reason,
ampicillin-sulbactam is no longer recom-
mended for treatment of community-
acquired intra-abdominal infections be-
cause of significant increased resistance in
E. coli.48 As mentioned above, targeted
anaerobic antimicrobial therapy should
be used in women with a TOA. Clindamy-
cin is generally recommended because this
was the agent used in the prior studies and
the agent in which clinicians have the most
experience. Although resistance to clinda-
mycin has been observed in isolates recov-
ered from the lower genital tract in women
with vaginitis,49 the significance of these
finding in women with TOA is uncertain as
there are no data suggesting higher failure
rates with clindamycin-based regimens.
Antibiotic therapy can be switched
from parenteral to oral route of admin-
istration after 24 hours of clinical im-
provement, resolution of nausea and
vomiting and severe pain. Patients should
complete an entire 14-day course of anti-
biotics with oral doxycycline. When a
TOA is present or when the illness was
preceded by gynecologic procedure great-
er anaerobic coverage is required, thus we
recommend the addition of clindamycin
or metronidazole to doxycycline. We pre-
fer to use metronidazole because of the
increased risk of Clostridium difficile col-
itis with clindamycin.
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Intrauterine Contraceptive
Device (IUCD) In Situ
When PID occurs with an IUCD in place
removal of the IUCD is not required.5052
However, 1 randomized study showed
that removal of the IUCD before the
initiation of antibiotic increased the rate
of clinical recovery.53 The availability of
alternative methods of contraception and
IUCD replacement should be considered
in the decision to remove the IUCD.
Women with PID and an IUCD in place
should have close clinical follow-up.
When the IUCD is removed, it should
not be replaced until 3 months after the
PID has resolved.
Surgical Management and
Drainage of TOAs
In general, the decision to combine anti-
microbial therapy with drainage or surgi-
cal excision of the TOA depends on the
status of the patient and the size of the
abscess. Antibiotics should be initiated as
soon as the diagnosis of TOA is deter-
mined. When rupture of a TOA is sus-
pected prompt surgical intervention is
required because of the morbidity and
mortality associated with a ruptured
TOA.54 Signs of sepsis, such as hypoten-
sion, tachycardia, and tachypnea, and an
acute abdomen are indicative of rupture,
and such patients should immediately
proceed to the operating room for surgi-
cal exploration.
TOAs usually present without evidence
of rupture and in these cases the role for
drainage or operative management of
TOA is less clear. Large case series have
shown that antimicrobial therapy alone
is usually effective in 70% of all
TOAs12,24,36,55,56 and in a few of these
studies abscess size has been shown to be
predictive of treatment success with anti-
biotics alone. Reed et al in 199145 showed
that 35% of abscesses 7 to 9 cm in size
required surgery as compared to almost

60% of abscesses >9 cm. DeWitt et al57
showed that abscesses >8 cm more often
required drainage or surgery and were
associated with longer length of hospital-
ization. Thus, it is reasonable to initiate
antibiotics alone in women who are
hemodynamically stable and when the
abscess is 8 cm or less in diameter. When
clinical response is not achieved within 48
hours after initiation of antibiotics, then
surgical management or drainage should
be considered. In addition, in women with
an abscess 8 cm or greater immediate
drainage rather awaiting clinical response
may decrease duration of hospitalization.
In addition, aggressive surgical manage-
ment should be considered in postmeno-
pausal women, because malignancy is a
concern in any postmenopausal woman
who presents with an abscess.5860 Proto-
papas et al59 reported that 8 of 17 (47%)
postmenopausal women had an underly-
ing malignancy as compared with 1 of
76 premenopausal women (1.3%). Thus,
postmenopausal women with TOA should
be counseled on their risk of malignancy
and potential need for complete surgical
staging. Although the diagnostic yield
could be lower in these cases due to the
significant necrosis of the tissue, a frozen
section of the abscess should be sent from
the operating room.
Surgical management options for TOAs
range from only drainage to unilateral
salpingo-operectomy to total abdominal
hysterectomy and bilateral salpingo-oo-
pherecectomy. Historically, most women
with TOA were managed aggressively with
a total abdominal hysterectomy and bilat-
eral salpingo-opherectomy. Although this
approach offered high cure rates, it was
at the cost of high rates of surgical com-
plications, infertility, and hormone defi-
ciency.61 With the advent of effective
antimicrobial therapy, operative manage-
ment has become much more conservative
moving toward procedures that allow
for sparing of ovarian function and if
possible can even be considered in cases
Severe Pelvic Inflammatory Disease 899
of rupture.24 Options for approach can
range from imaging-guided drainage to
laparoscopy to laparotomy. Most gynecol-
ogists continue to use the laparotomy as
the preferred surgical approach for de-
bridement of TOA. However, the laparo-
scopic approach seems to be safe in cases
where there is no evidence of TOA rupture
and may have improved outcomes of lap-
arotomy, including decreased length of
hospitalization, decreased rates of wound
infections, and more rapid rate of fever
defervesce.62 However, the surgical ap-
proach should depend on the skill and
comfort of the surgeon. Surgeries for
TOAs can be very complicated because
of the extensive adhesions from the abscess
to the surround structures and the necrotic
and inflamed tissues surrounding the ab-
scess. For this reason, the laparoscopic
experience and expertise of the surgeon
cannot be understated. We recommend
the removal of the abscess cavity and the
associated necrotic tissue and then irriga-
tion of the peritoneum. We offer hysterec-
tomy with bilateral salpingo-opherectomy
to patients who are acutely ill and have
completed child bearing. This approach
may hasten recovery compared with fertil-
ity-sparing surgery. In addition, this elim-
inates the need for repeat surgery that is
required in 10% to 20% of women who
have more conservative approaches.24,55
Since the 1970s, several imaging mo-
dalities and approaches have been used to
successfully drain intra-abdominal ab-
scess collections eliminating the need for
surgery.12,63,64 Pelvic abscess have been
drained using ultrasound or CT guidance
with a transabdominal, trangluteal, trans-
rectal, or transvaginal approach. The ap-
proach depends on the location of the
collection, with most commonly a trans-
abdominal approach for abscesses in the
upper pelvis or abdomen and a transva-
ginal approach for deeper pelvic ab-
scesses.65 Abscesses can be drained with
a catheter placement or aspiration alone
with a success rate ranging between
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900 Chappell and Wiesenfeld
77.8% and 100%.66 In a prospective
randomized trial comparing treatment of
TOA with antibiotics alone or antibiotics
with aspiration of the abscess, 17 of
20 women responded in the aspiration
group, whereas only 10 of 20 responded
in the antibiotics alone group. In addi-
tion, time to discharge was much shorter
in the aspiration group when compared
with the antibiotics alone group, 3.9 ver-
sus 9.1 days, respectively.67 Gjelland and
colleagues reported a cohort of 302 wom-
en with TOAs treated with antibiotics
combined with ultrasound-guided trans-
vaginal aspiration of the abscess with a
success rate of 93.4%. They repeated the
aspiration if abscess material was still seen
on ultrasound 2 to 4 days after initial
aspiration. They reported complete pain
relief in 62.3% of the women within 48
hours of the first aspiration and no pro-
cedure-related complications. Only 6%
of this cohort of women ultimately re-
quired surgery.32 The optimal approach
for management of TOA is still debatable.
However, in institutions where there are
radiologists trained to do these proce-
dures, it seems advantageous to consider
transvaginal aspiration of the abscess in
combination with standard antibiotics,
particularly with larger abscesses, as this
may increase the response rate, decrease
the length of hospitalization, and improve
pain control.
Long-term Complications
Although prompt diagnosis and treat-
ment decreases the risk of long-term com-
plications of PID, many women, despite
adequate treatment, still suffer from re-
current PID, infertility, ectopic preg-
nancy, and chronic pelvic pain. These
complications are attributable to scarring
and adhesion formation that accompany
the healing of tissues that were damaged
initially at the time of acute infection. One
study reported that 15% of women had a
recurrence within 35 months and 21% of
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women had a recurrence within 84
months.68 Westrom and colleagues fol-
lowed a cohort of 415 women with visu-
ally confirmed PID and found that on
average 21% of the women had infertility.
The most important predictor of infertil-
ity was reinfection: 12.8% with a single
episode, 35.5% with 2 episodes, and 75%
with Z3 episodes. In addition, they noted
that the severity of the initial PID case was
a predictor of fertility outcome; with in-
fertility rates of 2.6%, 13.1%, and 28.6%
for mild, moderate, and severe disease,
respectively.17 Chlamydial infection and
delay in seeking care are also known risk
factors for infertility in women with
PID.69,70 The incidence of ectopic preg-
nancy in the first pregnancy after PID was
7.8% as compared with 1.3% of women
without a history of PID.71 In addition to
complications related to pregnancy out-
comes, the scarring and adhesions caused
by PID may also lead to chronic pelvic
pain in women with a prior history of
PID. Up to one third of women with a
history of PID go on to develop chronic
pelvic pain.37,72 Similar to the risks of
infertility, the number of PID recurrences
was the strongest predictor for the devel-
opment of chronic pelvic pain.73
Conclusions
Severe PID and PID associated with TOA
contribute significantly to the number of
patients with pelvic infections admitted to
the hospital. These diagnoses are associ-
ated with significant long-term morbidity,
including poor reproductive outcomes
and chronic pain. A high level of suspicion
for TOAs in women with PID is required,
as many women with TOAs do not have
fever or an elevated white cell count.
Women with TOAs should be admitted
to the hospital and immediately started
in IV antibiotics that cover enteric
Gram-negative rods (a virulent cause of
sepsis) and anaerobic bacteria (especially
in the cases of TOAs). Percutaneous

radiologic-guided drainage plays an im-
portant role in the management of TOAs,
particularly if the abscess is large. Im-
mediate surgical management should
always be performed in cases suspected
of rupture.
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